Burst-suppression EEG Pattern Research Articles

Electroencephalographic guided propofol-remifentanil TCI anesthesia with and without dexmedetomidine in a geriatric population: electroencephalographic signatures and clinical evaluation.

Elderly and multimorbid patients are at high risk for developing unfavorable postoperative neurocognitive outcomes; however, well-adjusted and EEG-guided anesthesia may help titrate anesthesia and improve postoperative outcomes. Over the last decade, dexmedetomidine has been increasingly used as an adjunct in the perioperative setting. Its synergistic effect with propofol decreases the dose of propofol needed to induce and maintain general anesthesia. In this pilot study, we evaluate two highly standardized anesthetic regimens for their potential to prevent burst suppression and postoperative neurocognitive dysfunction in a high-risk population. Prospective, randomized clinical trial with non-blinded intervention. Operating room and post anesthesia care unit at Hospital Base San José, Osorno/Universidad Austral, Valdivia, Chile. 23 patients with scheduled non-neurologic, non-cardiac surgeries with age > 69years and a planned intervention time > 60min. Patients were randomly assigned to receive either a propofol-remifentanil based anesthesia or an anesthetic regimen with dexmedetomidine-propofol-remifentanil. All patients underwent a slow titrated induction, followed by a target controlled infusion (TCI) of propofol and remifentanil (n = 10) or propofol, remifentanil and continuous dexmedetomidine infusion (n = 13). We compared the perioperative EEG signatures, drug-induced changes, and neurocognitive outcomes between two anesthetic regimens in geriatric patients. We conducted a pre- and postoperative Montreal Cognitive Assessment (MoCa) test and measured the level of alertness postoperatively using a sedation agitation scale to assess neurocognitive status. During slow induction, maintenance, and emergence, burst suppression was not observed in either group; however, EEG signatures differed significantly between the two groups. In general, EEG activity in the propofol group was dominated by faster rhythms than in the dexmedetomidine group. Time to responsiveness was not significantly different between the two groups (p = 0.352). Finally, no significant differences were found in postoperative cognitive outcomes evaluated by the MoCa test nor sedation agitation scale up to one hour after extubation. This pilot study demonstrates that the two proposed anesthetic regimens can be safely used to slowly induce anesthesia and avoid EEG burst suppression patterns. Despite the patients being elderly and at high risk, we did not observe postoperative neurocognitive deficits. The reduced alpha power in the dexmedetomidine-treated group was not associated with adverse neurocognitive outcomes.

Utility and limitations of EEG in the diagnosis and management of ALDH7A1-related pyridoxine-dependent epilepsy. A retrospective observational study.

Pyridoxine-dependent epilepsy due to ALDH7A1 variants (PDE-ALDH7A1) is a rare disorder, presenting typically with severe neonatal, epileptic encephalopathy. Early diagnosis is imperative to prevent uncontrolled seizures. We have explored the role of EEG in the diagnosis and management of PDE. A total of 13 Norwegian patients with PDE-ALDH7A1 were identified, of whom five had reached adult age. Altogether 163 EEG recordings were assessed, 101 from the 1st year of life. Median age at seizure onset was 9 h (IQR 41), range 1 h-6 days. Median delay from first seizure to first pyridoxine injection was 2 days (IQR 5.5). An EEG burst suppression pattern was seen in eight patients (62%) during the first 5 days of life. Eleven patients had recordings during pyridoxine injections: in three, immediate EEG improvement correlated with seizure control, whereas in six, no change of epileptiform activity occurred. Of these six, one had prompt clinical effect, one had delayed effect (< 1 day), one had no effect, one had uncertain effect, and another had more seizures. A patient without seizures at time of pyridoxine trial remained seizure free for 6 days. Two patients with prompt clinical effect had increased paroxysmal activity, one as a conversion to burst suppression. Autonomic seizures in the form of apnoea appeared to promote respiratory distress and were documented by EEG in one patient. EEG follow-up in adult age did not show signs of progressing encephalopathy. A neonatal burst suppression EEG pattern should raise the suspicion of PDE-ALDH7A1. Respiratory distress is common; isolated apnoeic seizures may contribute. EEG responses during pyridoxine trials are diverse, often with poor correlation to immediate clinical effect. Reliance on single trials may lead to under-recognition of this treatable condition. Pyridoxine should be continued until results from biomarkers and genetic testing are available.

The dosage of thiopental as pharmacological cerebral protection during non-shunt carotid endarterectomy: A retrospective study.

Thiopental has been used as a pharmacological cerebral protection strategy during carotid endarterectomy surgeries. However, the optimal dosage required to induce burst suppression on the electroencephalogram (EEG) remains unknown. This retrospective study aimed to determine the optimal dosage of thiopental required to induce burst suppression during non-shunt carotid endarterectomy. The Neurological Institute of Thailand Review Board approved the study. Data were collected from 2009 to 2019 for all non-shunt carotid endarterectomy patients who received thiopental for pharmacological cerebral protection and had intraoperative EEG monitoring. Demographic information, carotid stenosis severity, intraoperative EEG parameters, thiopental dosage, carotid clamp time, intraoperative events, and patient outcomes were abstracted. The study included 57 patients. Among them, 24 patients (42%) achieved EEG burst suppression pattern with a thiopental dosage of 26.3±10.1 mg/kg/hr. There were no significant differences in perioperative events between patients who achieved burst suppression and those who did not. After surgery, 33.3% of patients who achieved burst suppression were extubated and awakened. One patient in the non-burst suppression group experienced mild neurological deficits. No deaths occurred within one month postoperative. The optimal dosage of thiopental required to achieve burst suppression on intraoperative EEG during non-shunt carotid endarterectomy was 26.3±10.1 mg/kg/hr.

The dosage of thiopental as pharmacological cerebral protection during non-shunt carotid endarterectomy: A retrospective study

Background: Thiopental has been used as a pharmacological cerebral protection strategy during carotid endarterectomy surgeries. However, the optimal dosage required to induce burst suppression on the electroencephalogram (EEG) remains unknown. This retrospective study aimed to determine the optimal dosage of thiopental required to induce burst suppression during non-shunt carotid endarterectomy. Methods: The Neurological Institute of Thailand Review Board approved the study. Data were collected from 2009 to 2019 for all non-shunt carotid endarterectomy patients who received thiopental for pharmacological cerebral protection and had intraoperative EEG monitoring. Demographic information, carotid stenosis severity, intraoperative EEG parameters, thiopental dosage, carotid clamp time, intraoperative events, and patient outcomes were abstracted. Results: The study included 57 patients. Among them, 24 patients (42%) achieved EEG burst suppression pattern with a thiopental dosage of 26.3+10.1 mg/kg/hr. There were no significant differences in perioperative events between patients who achieved burst suppression and those who did not. After surgery, 33.3% of patients who achieved burst suppression were extubated and awakened. One patient in the non-burst suppression group experienced mild neurological deficits. No deaths occurred within one month postoperative. Conclusions: The optimal dosage of thiopental required to achieve burst suppression on intraoperative EEG during non-shunt carotid endarterectomy was 26.3+10.1 mg/kg/hr.

The dosage of thiopental as pharmacological cerebral protection during non-shunt carotid endarterectomy: A retrospective study

Background: Thiopental has been used as a pharmacological cerebral protection strategy during carotid endarterectomy surgeries. However, the optimal dosage required to induce burst suppression on the electroencephalogram (EEG) remains unknown. This retrospective study aimed to determine the optimal dosage of thiopental required to induce burst suppression during non-shunt carotid endarterectomy. Methods: The Neurological Institute of Thailand Review Board approved the study. Data were collected from 2009 to 2019 for all non-shunt carotid endarterectomy patients who received thiopental for pharmacological cerebral protection and had intraoperative EEG monitoring. Demographic information, carotid stenosis severity, intraoperative EEG parameters, thiopental dosage, carotid clamp time, intraoperative events, and patient outcomes were abstracted. Results: The study included 57 patients. Among them, 24 patients (42%) achieved EEG burst suppression pattern with a thiopental dosage of 26.3+10.1 mg/kg/hr. There were no significant differences in perioperative events between patients who achieved burst suppression and those who did not. After surgery, 33.3% of patients who achieved burst suppression were extubated and awakened. One patient in the non-burst suppression group experienced mild neurological deficits. No deaths occurred within one month postoperative. Conclusions: The optimal dosage of thiopental required to achieve burst suppression on intraoperative EEG during non-shunt carotid endarterectomy was 26.3+10.1 mg/kg/hr.

Association Between Induced Burst Suppression and Clinical Outcomes in Patients With Refractory Status Epilepticus: A 9-Year Cohort Study.

To investigate the frequency of induced EEG burst suppression pattern during continuous IV anesthesia (IVAD) and associated outcomes in adult patients treated for refractory status epilepticus (RSE). Patients with RSE treated with anesthetics at a Swiss academic care center from 2011 to 2019 were included. Clinical data and semiquantitative EEG analyses were assessed. Burst suppression was categorized as incomplete burst suppression (with ≥20% and <50% suppression proportion) or complete burst suppression (with ≥50% suppression proportion). The frequency of induced burst suppression and association of burst suppression with outcomes (persistent seizure termination, in-hospital survival, and return to premorbid neurologic function) were the endpoints. We identified 147 patients with RSE treated with IVAD. Among 102 patients without cerebral anoxia, incomplete burst suppression was achieved in 14 (14%) with a median of 23 hours (interquartile range [IQR] 1-29) and complete burst suppression was achieved in 21 (21%) with a median of 51 hours (IQR 16-104). Age, Charlson comorbidity index, RSE with motor symptoms, the Status Epilepticus Severity Score and arterial hypotension requiring vasopressors were identified as potential confounders in univariable comparisons between patients with and without any burst suppression. Multivariable analyses revealed no associations between any burst suppression and the predefined endpoints. However, among 45 patients with cerebral anoxia, induced burst suppression was associated with persistent seizure termination (72% without vs 29% with burst suppression, p = 0.004) and survival (50% vs 14% p = 0.005). In adult patients with RSE treated with IVAD, burst suppression with ≥50% suppression proportion was achieved in every fifth patient and not associated with persistent seizure termination, in-hospital survival, or return to premorbid neurologic function.

Balancing the risks and benefits of anesthetics in status epilepticus

PurposeAccording to international guidelines, status epilepticus refractory to first- and second-line antiseizure medication should be treated with anesthetics. Therefore, continuously delivered intravenous midazolam, propofol, or barbiturates are recommended as third-line therapy. While electroencephalographically (EEG)-controlled titration of anesthetics to seizure termination or to the emergence of an EEG burst-suppression pattern makes sense, evidence of the efficacy and tolerability of such third-line treatment is limited and concerns regarding the risks of anesthesia remain. The lack of treatment alternatives and persistent international discord reflecting contradictory results from some studies leave clinicians on their own when deciding to escalate treatment.In this conference-accompanying narrative review, we highlight the challenges of EEG-monitored third-line treatment and discuss recent studies that examined earlier administration of anesthetics. ResultsBased on the literature, maintaining continuous burst suppression is difficult despite the constant administration of anesthetics, and the evidence for burst suppression as an adequate surrogate target is limited by methodological shortcomings as acknowledged by international guidelines. In our Swiss cohort including 102 patients with refractory status epilepticus, burst suppression as defined by the American Clinical Neurophysiology Society's Critical Care EEG Terminology 2021 was established in only 21%. Besides case reports suggesting that rapid but short-termed anesthesia can be sufficient to permanently stop seizures, a study including 205 patients revealed that anesthesia as second-line treatment was associated with a shorter median duration of status epilepticus (0.5 versus 12.5 days, p < 0.001), median ICU (2 versus 5.5 days, p < 0.001) and hospital stay (8 versus 17 days, p < 0.001) with equal rates of complications when compared to anesthesia as third-line treatment. ConclusionsRecent investigations have led to important findings and new insights regarding the use of anesthetics in refractory status epilepticus. However, numerous methodological limitations and remaining questions need to be considered when it comes to the translation into clinical practice, and, in consequence, call for prospective randomized studies.This paper was presented at the 8th London-Innsbruck Colloquium on Status Epilepticus and Acute Seizures held in September 2022.

Therapeutically induced EEG burst-suppression pattern to treat refractory status epilepticus—what is the evidence?

AbstractCurrent guidelines advocate to treat refractory status epilepticus (RSE) with continuously administered anesthetics to induce an artificial coma if first- and second-line antiseizure drugs have failed to stop seizure activity. A common surrogate for monitoring the depth of the artificial coma is the appearance of a burst-suppression pattern (BS) in the EEG. This review summarizes the current knowledge on the origin and neurophysiology of the BS phenomenon as well as the evidence from the literature for the presumed benefit of BS as therapy in adult patients with RSE.

Etiology of Burst Suppression EEG Patterns.

Burst-suppression electroencephalography (EEG) patterns of electrical activity, characterized by intermittent high-power broad-spectrum oscillations alternating with isoelectricity, have long been observed in the human brain during general anesthesia, hypothermia, coma and early infantile encephalopathy. Recently, commonalities between conditions associated with burst-suppression patterns have led to new insights into the origin of burst-suppression EEG patterns, their effects on the brain, and their use as a therapeutic tool for protection against deleterious neural states. These insights have been further supported by advances in mechanistic modeling of burst suppression. In this Perspective, we review the origins of burst-suppression patterns and use recent insights to weigh evidence in the controversy regarding the extent to which burst-suppression patterns observed during profound anesthetic-induced brain inactivation are associated with adverse clinical outcomes. Whether the clinical intent is to avoid or maintain the brain in a state producing burst-suppression patterns, monitoring and controlling neural activity presents a technical challenge. We discuss recent advances that enable monitoring and control of burst suppression.

Long-term prognosis related to deep sedation in refractory status Epilepticus.

To evaluate long-term prognosis in patients with refractory status epilepticus according to the level of sedation reached during drug-induced coma. Longitudinal study of patients with status epilepticus who received anesthetics to induce therapeutic coma. Demographic data, clinical, and electroencephalographic characteristics were collected, as well as variables related to sedation. We considered as deep sedation the EEG burst-suppression patterns (suppression ratio>50%). A GOSE (Glasgow Outcome Scale Extended) score of 7 or 8 was considered as good prognosis. A comparative study was carried out to identify predictors of good or poor prognosis at discharge, at 1 and 2years of follow-up. We included 61 patients: 63.9% were men; mean age 53.5±16.8years (range 16-86years), 39.3% reached deep sedation; 62.3% had>48 h induced coma. The median hospital stay was 21days, while 10days in the intensive care unit (ICU). In the multiple regression analysis, an ICU length of stay≥7days was associated with poor prognosis at discharge and at long-term (P<.05), while deep sedation was associated only with poor long-term prognosis (1 and 2years, P<.05). The Kaplan-Meier curve showed higher survival in the group that did not undergo deep sedation (P<.05). In refractory status epilepticus, deep sedation is associated with poor prognosis at long-term.

P16-F Generation of burst-suppression pattern on electroencephalography and electrocorticography in general anesthesia: Dose–effect relationship

Background Electroencephalographic (EEG) patterns of brain electrical activity (BEA) reflect the level of anesthesia during neurosurgery. Excessive levels of anesthesia are accompanied by burst-suppression pattern (BSP) or even electrical inactivity. Moderate anesthesia is necessary to ensure optimal results of intraoperative motor mapping. We aimed to determine median effective doses (ED50) for propofol or sevoflurane anesthesia that are associated with BSP in EEG and electrocorticographic (ECoG) recordings. Material and methods Data of 60 patients (m/f = 32/28, age 21–65, BMI Results ED50 of anesthetics for EEG were greater than those for ECoG for both drugs. ED50 for propofol equaled 4.6 ± 0.4 mg/kg/h for ECoG and 6.9 ± 0.9 mg/kg/h for EEG. Median MAC of sevoflurane was 0.51 ± 0.16 for ECoG and 1.08 ± 0.18 for EEG. Conclusions EEG-based techniques for anesthesia level assessment may be less sensitive than ECoG-based.

Burst-suppression eeg pattern is not always a predictor of poor prognosis in children

Burst-suppression eeg pattern is not always a predictor of poor prognosis in children

Holding on by a Breath: Carbamazepine Overdose and Neurologic Dysfunction

SESSION TITLE: Critical Care 1 SESSION TYPE: Affiliate Case Report Slide PRESENTED ON: Sunday, October 29, 2017 at 10:45 AM - 12:00 PM INTRODUCTION: Carbamazepine overdose is known to cause coma, however continuous electroencephalogram (cEEG) findings of a burst suppression pattern are rare. We report a case of carbamazepine overdose with cranial nerve (CN) areflexia, cEEG burst suppression pattern, and brain death mimicry with complete neurologic recovery. CASE PRESENTATION: A 54-year-old woman with a history of bipolar disorder was found unresponsive by her husband. An empty bottle of carbamazepine was identified by medical personnel. She was intubated for respiratory depression, and a neurological assessment revealed an absence of CN reflexes. Her initial carbamazepine level was 15ug/mL and peaked at 57ug/mL. There was concern for severe anoxic brain injury due to periods of apnea on the ventilator and complete CN areflexia. A cEEG revealed a burst suppression pattern. A computed tomography scan showed diffuse cerebral edema. Intermittent dialysis was initiated for treatment of severe carbamazepine toxicity. Five days following initial presentation, she regained all her CN reflexes. On day seven, she was extubated with complete neurological recovery and no evidence of neurological sequela. DISCUSSION: Carbamazepine is a frequently prescribed medication with well-known side effects. Carbamazepine toxicity producing CN areflexia with EEG burst suppression pattern has not been well described. A review of the literature revealed one case report of a patient presenting with burst suppression pattern, abundant epileptiform activity, and generalized seizures which resolved within 24 hours. Unfortunately, the patient expired and clinical correlation based on cEEG improvement could not be ascertained. In contrast, our patient had a prolonged course of CN areflexia and burst suppression, with complete neurological recovery. Typically, prolonged areflexia and an EEG burst suppression pattern are predictors of poor outcome in hypoxic-ischemic brain injuries. However, these predictors have not been well studied in patients with carbamazepine toxicity. CONCLUSIONS: Our case illustrates that CN areflexia and an EEG burst suppression pattern in carbamazepine toxicity may not be predictive of neurological outcome. Clinicians must be aware of the potentially reversible neurological sequelae following carbamazepine toxicity and refrain from early prognostication in this group of patients. Reference #1: De Rubeis DA, et al. Continuous EEG Monitoring in a Patient With Massive Carbamazepine Overdose, Journal of Clinical Neurophysiology 18(02):166-168 DISCLOSURE: The following authors have nothing to disclose: Susannah Kurtz, Adiac Espinosa Hernandez, Ismini Kourouni, Karishma Parekh, James Salonia No Product/Research Disclosure Information

A de novo missense mutation of GABRB2 causes early myoclonic encephalopathy

BackgroundEarly myoclonic encephalopathy (EME), a disease with a devastating prognosis, is characterised by neonatal onset of seizures and massive myoclonus accompanied by a continuous suppression-burst EEG pattern. Three genes are...

Autopsy findings of a patient with acute encephalitis and refractory, repetitive partial seizures

Chikako Ogawa *, Jun Natsume , Hiroyuki Yamamoto , Naoko Ishihara , Atsushi Tashiro , Hiroyuki Kidokoro , Tamiko Negoro , Mari Yoshida , Kazuyoshi Watanabe a Department of Pediatrics, Nagoya University Graduate School of Medicine, Nagoya, Japan Department of Pediatrics, Social Insurance Chukyo Hospital, Nagoya, Japan Department of Neuropathology, Institute for Medical Science of Aging, Aichi Medical University, Nagakute, Japan

Early Infantile Epileptic Encephalopathy with a de novo variant in ZEB2 identified by exome sequencing

Early Infantile Epileptic Encephalopathy (EIEE) presents shortly after birth with frequent, severe seizures, a burst-suppression EEG pattern, and progressive disturbance of cerebral function. We present a case of EIEE associated with a de novo missense variant in ZEB2. Heterozygous truncating mutations or deletions in ZEB2 are known to cause Mowat-Wilson syndrome (MWS), which is characterized by seizures with onset in the second year of life, distinctive dysmorphic facial features and malformations that were absent in this patient. This unique case expands the range of phenotypes associated with variants in ZEB2 and indicates that this gene should be included in the molecular investigation of EIEE cases.

Electroencephalography During Hemiarch Replacement With Moderate Hypothermic Circulatory Arrest

This study aimed to characterize intraoperative electroencephalography (EEG) during moderate hypothermic circulatory arrest (MHCA) with selective antegrade cerebral perfusion (SACP), which has not been described previously. This was a single-institution retrospective study of patients undergoing aortic hemiarch replacement using MHCA (temperatures <28°C at circulatory arrest [CA]) and unilateral SACP with EEG monitoring from July 1, 2013 to November 1, 2014. The EEG pattern was determined before and immediately after CA, as well as after establishment of SACP. Patient and procedural characteristics and outcomes were determined and compared after stratification by the presence of ischemic EEG changes. The study included 71 patients. Before CA, 47patients (66%) demonstrated a continuous EEG pattern, with or without periodic complexes, and 24 (34%) had a burst suppression EEG pattern. Immediately after CA, abrupt loss of electrocerebral activity occurred in 32patients (45%), suggestive of cerebral ischemia. Establishment of unilateral SACP rapidly restored electrocerebral activity in all but 2 patients. One patient had persistent loss of left-sided activity, which resolved after transition to bilateral SACP. Another patient had persistent global loss of activity and was placed back on cardiopulmonary bypass for further cooling before reinitiation of CA. No significant differences in characteristics or outcomes were assessed between patients with and without loss of EEG activity. Nearly half of patients undergoing hemiarch replacement with MHCA/SACP experience abrupt loss of electrocerebral activity after CA is initiated. Although unilateral SACP usually restores prearrest electrocerebral activity, intraoperative EEG may be particularly valuable for the identification of patients with persistent cerebral ischemia even after SACP.

EEG and the newborn

Despite the evolution of new technologies for assessing neonatal brain function, electroencephalography (EEG) remains a powerful tool for neurological diagnosis and prognosis in neonates. It is considered the gold standard for distinguishing epileptic seizures from non-epileptic paroxysmal events and for detecting subclinical seizure activity in high-risk babies. In those babies severely ill, EEG is even more efficient as predictive test than the neurological examination. The prognostic value of neonatal EEG has been long recognized in term as well as in preterm infants. Background patterns, more that patterns of ictal discharges, correlate significantly with the long-term outcome. Although most abnormalities on the neonatal EEG are nonspecific, certain patterns can be highly suggestive for diagnosis. Prognostic value can be increased by obtaining early recordings, possibly within the first 48 hr of life, prolonged recordings to include samples of different activity states, and serial EEGs at short intervals to assess rapid changes that are likely to occur in high-risk infants. It is important to distinguish neonatal seizures from neonatal-onset epilepsies and epilepsy syndromes. Both benign and malignant neonatal epilepsy syndromes exist. While benign familial neonatal seizures represents a neonatal syndrome with benign outcome, early myoclonic encephalopathy and Ohtahara syndrome are the earliest form of age-dependent severe epilepsy syndromes. Early myoclonic encephalopathy and Ohtahara syndrome are both characterized by the presence of a burst-suppression EEG pattern. This pattern is usually associated with a poor prognosis and is considered the electroencephalographic correlate of a complete disconnection within the thalamocortical systems. Migrating partial seizures in infancy is a newly recognized epilepsy syndrome whose onset can be in the neonatal period. It is characterized by multifocal intractable seizures associated with psychomotor impairment. No etiology has been found so far. Different drugs currently used in neonatal intensive care unit, especially if in the toxic range, can alter the EEG background. Those effects need to be taken in account in the interpretation of neonatal EEG.

Hemoglobin Concentration Affects Electroencephalogram During Cardiopulmonary Bypass: An Indication for Neuro-Protective Values.

Hemodilution during cardiopulmonary bypass (CPB) is widely used to decrease transfusion and improve microcirculation but has drawbacks, such as diminished hemoglobin levels. Among others, reduced brain oxygenation accounts for neurological adverse outcomes after CPB. The aim of the present study was to ascertain if and how continuous electroencephalogram (EEG) during CPB is affected by hematocrit level and what should be the minimum value to avoid significant frequency band shifts on the EEG. A comparative study design was used with 16 subjects undergoing elective mitral valve repair/replacement. EEG was continuously recorded during the surgical procedure (from anesthesia induction to 20 min after CPB end). Data were marked at relevant time points (T0: before CPB start; T1: after 30 min from CPB beginning; T2: at CPB end), and the following 2 min EEG analyzed with a fast Fourier transform to obtain relative power for delta, theta, alpha, and beta bands. A general linear model for repeated measure was used to study interactions of time (T0, T1, and T2, EEG frequency band, and topographical distribution. The relative powers for each electrode were calculated and represented using topographic maps. Power spectrum differences between time points (T2-T1; T2-T0; T1-T0) were calculated for each electrode, and differences >10%, considered indicative of neuronal sufferance, were included in further analysis. Cutoff hemoglobin values that maximize the proportion of correctly classified EEG band shifts were obtained by previous definition were obtained. At T2, diffuse EEG slowing in delta and theta bands was detected; a minor slowing over anterior regions was evident at T1 for the theta band. Decrements in EEG power greater than 10% were detected only for the delta band at T2. Hemoglobin concentration levels at which no slowing increase was evident were 9.4 mg/dL (Ht: 28.2%) at T1 and 9.2 mg/dL (Ht: 27.6%) at T2. EEG burst-suppression pattern related to a lesser degree of slowing at T2. In conclusion, we propose hemoglobin cutoff levels that prevent EEG slowing indicative of neuronal sufferance. In addition, burst-suppression EEG patterns offer higher central nervous system protection as measured on EEG.

Neuronal networks in burst suppression EEG patterns in newborns as revealed by source analysis

Neuronal networks in burst suppression EEG patterns in newborns as revealed by source analysis